COMPLETE BLOCK OF EARLY B-CELL DIFFERENTIATION AND ALTERED PATTERNINGOF THE POSTERIOR MIDBRAIN IN MICE LACKING PAX5 BSAP/

The Pax5 gene, coding for the transcription factor BSAP, was mutated i n the mouse germline by targeted disruption. Homozygous mutant mice we re born alive, became growth retarded, and usually died within three w eeks. About 5% of mutants survived to adulthood and were fertile, but severely runted. Morphogenesis of the posterior midbrain was affected as early as embryonic day 16.5, leading to a reduction of the inferior colliculus near the midline and to altered foliation of the anterior cerebellum. Moreover, all mutants failed to produce small pre-B, B, an d plasma cells owing to a complete arrest of B cell development at an early precursor stage. These data define a key role for Pax5 in early a lymphopoiesis and midbrain patterning.